Degeneration of nerve cells in the brain is responsible for many disorders. Such disorders include Parkinson's disease, Huntington's disease, Alzheimer's disease, and the pathology associated with stroke and cerebral ischemia, and often include symptoms of tremor and spasticity. Excessive stimulation of receptors by the endogenous excitatory amino acids, glutamate and aspartate, is known to produce neuronal loss and to mimic many of the symptoms of these disorders. Similarly, administration of glutamate agonists such as quinolinic acid, kainic acid, and. quisqualic acid to rodents has been shown to cause neuronal degeneration. The patterns of this loss have been compared to the neuronal loss accompanying neurodegenerative disorders such as Huntington's disease, parkinsonism and Alzheimer's disease in humans, suggesting that rapid and excessive release of endogenous glutamate, which acts as a toxin, is the common cause of the neurological symptoms arising from diverse disease processes, and indicating that antagonists of excitatory amino acids will be useful in the treatment of neurodegenerative disorders. Compounds such as MK-801, i.e., (S)-10,11-dihydro-5-methyl-5H-dibenzo(a,d)cyclohepten-5,10-imine, that have have been shown either to antagonize the seizures induced in mice by quinolinic acid, a compound thought to be an agonist at the N-methyl-D-aspartate (NMDA)-subtype of the glutamate receptor, or to antagonize hippocampal neurodegeneration after carotid artery occlusion in gerbils, are being developed for use as neuroprotectants.